ArticleCurrent biology : CB2015
Aging Neural Progenitors Lose Competence to Respond to Mitogenic Notch Signaling.
Article in Current biology : CB, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- From the Making of a Neural Lineage to the Making of a Tumor: Lessons from the "Simple" Drosophila Brain.Advances in experimental medicine and biology · 2025Review
- Indirect neurogenesis in space and time.Nature reviews. Neuroscience · 2024Review
- A Notch-dependent transcriptional mechanism controls expression of temporal patterning factors ineLife · 2022Article
- Single cell RNA-seq analysis reveals temporally-regulated and quiescence-regulated gene expression in Drosophila larval neuroblasts.Neural development · 2022Article
- Non-autonomous regulation of neurogenesis by extrinsic cues: aOxford open neuroscience · 2022Review
- Cell-type-specific chromatin occupancy by the pioneer factor Zelda drives key developmental transitions in Drosophila.Nature communications · 2021Article
- Regulation of Neural Stem Cell Competency and Commitment during Indirect Neurogenesis.International journal of molecular sciences · 2021Review
- Structural aspects of the aging invertebrate brain.Cell and tissue research · 2021Review
- Temporal patterning in neural progenitors: fromDisease models & mechanisms · 2020Review
- Temporal identity establishes columnar neuron morphology, connectivity, and function in aeLife · 2019Article
- Article
- Lunatic fringe-mediated Notch signaling regulates adult hippocampal neural stem cell maintenance.eLife · 2017Article
- Asymmetric Notch Amplification to Secure Stem Cell Identity.Developmental cell · 2017Article
- Opportunities lost and gained: Changes in progenitor competence during nervous system development.Neurogenesis (Austin, Tex.) · 2017Review
- Notch signalling in context.Nature reviews. Molecular cell biology · 2016Review
- Notch maintains Drosophila type II neuroblasts by suppressing expression of the Fez transcription factor Earmuff.Development (Cambridge, England) · 2016Article
- Transgenic mouse models for studying adult neurogenesis.Frontiers in biology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Drosophila neural stem cells (neuroblasts) are a powerful model system for investigating stem cell self-renewal, specification of temporal identity, and progressive restriction in competence. Notch signaling is a conserved cue that is an important determinant of cell fate in many contexts across animal development; for example, mammalian T cell differentiation in the thymus and neuroblast specification in Drosophila are both regulated by Notch signaling. However, Notch also functions as a mitogen, and constitutive Notch signaling potentiates T cell leukemia as well as Drosophila neuroblast tumors. While the role of Notch signaling has been studied in these and other cell types, it remains unclear how stem cells and progenitors change competence to respond to Notch over time. Notch is required in type II neuroblasts for normal development of their transit amplifying progeny, intermediate neural progenitors (INPs). Here, we find that aging INPs lose competence to respond to constitutively active Notch signaling. Moreover, we show that reducing the levels of the old INP temporal transcription factor Eyeless/Pax6 allows Notch signaling to promote the de-differentiation of INP progeny into ectopic INPs, thereby creating a proliferative mass of ectopic progenitors in the brain. These findings provide a new system for studying progenitor competence and identify a novel role for the conserved transcription factor Eyeless/Pax6 in blocking Notch signaling during development.
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